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Research Article Free access | 10.1172/JCI115517

Endogenous adenosine is an autacoid feedback inhibitor of chloride transport in the shark rectal gland.

G G Kelley, O S Aassar, and J N Forrest Jr

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

Find articles by Kelley, G. in: PubMed | Google Scholar

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

Find articles by Aassar, O. in: PubMed | Google Scholar

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

Find articles by Forrest, J. in: PubMed | Google Scholar

Published December 1, 1991 - More info

Published in Volume 88, Issue 6 on December 1, 1991
J Clin Invest. 1991;88(6):1933–1939. https://doi.org/10.1172/JCI115517.
© 1991 The American Society for Clinical Investigation
Published December 1, 1991 - Version history
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Abstract

The present studies define the physiologic role of endogenous adenosine in the perfused shark rectal gland, a model epithelia for hormone-stimulated chloride transport. Chloride ion secretion, and venous adenosine and inosine concentrations increased in parallel in response to hormone stimulation. From a basal rate of 157 +/- 26 mu eq/h per g, chloride secretion increased to 836 +/- 96 and 2170 +/- 358 with 1 and 10 microM forskolin, venous adenosine increased from 5.0 +/- 1 to 126 +/- 29 and 896 +/- 181 nM, and inosine increased from 30 +/- 9 to 349 +/- 77 and 1719 +/- 454 nM (all P less than 0.01). Nitrobenzylthioinosine (NBTI), a nucleoside transport inhibitor, completely blocked the release of adenosine and inosine. Inhibition of chloride transport with bumetanide, an inhibitor of the Na+/K+/2Cl- cotransporter, or ouabain, an inhibitor of Na+/K+ ATPase activity, reduced venous adenosine and inosine to basal values. When the interaction of endogenous adenosine with extracellular receptors was prevented by adenosine deaminase, NBTI, or 8-phenyltheophylline, the chloride transport response to secretagogues increased by 1.7-2.3-fold. These studies demonstrate that endogenous adenosine is released in response to hormone-stimulated cellular work and acts at A1 adenosine receptors as a feedback inhibitor of chloride transport.

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